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MALIGNANT HEME > SET5 > Flashcards

SET5 Flashcards

1
Q

Which requires a longer maintenance tx, AML or ALL?

A

ALL- often get HyperCVAD alternating with HD MTX + Ara-C w/ intrathecal tx then followed by POMP maintenance Tx for 2-3 YEARS

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2
Q

What kind of consolidation should be done in AML t(6;9)?

A

Allo-HSCT in first remission due to poor risk cytogenetic; if no donor can do HiDAC but really try for alloHSCT asap

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3
Q

What CD markers are associated with AML M7?

A

CD 41 + CD61, note these are also associated with GpIIb/IIIa which is the target of plavix; makes sense as M7 is megakaryoblastic AML

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4
Q

What percent of quantitative BCR-ABL transcript predicts for relapse in in Ph + ALL?

A

>0.1 %; if this is the case then the patient should undergo an allo-HSCT

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5
Q

This class of drug is notorious for causing mutations in the MLL (Mixed Lineage Leukemia) gene at the 11q23 locus leading ot MDS 1-3 years later

A

Topoisomerase II inhibitor (Etoposide)

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6
Q

Deletions of chromosome 5 and 7 are often seen in AML with what previous treatement?

A

Anthracyclines

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7
Q

What is HyperCVAD?

A

Hyperfractionated Cyclophosphamide, Vincristine, Adriamycin, and dexamethasone alternating with HD MTX and cytarabine

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8
Q

ALL with EPOR or JAK2 rearrangements is a type of Philadelphia-positive-like ALL sensitive to _______

A

Ruxolitinib

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9
Q

Why is Blinatumumab only used in B cell ALL

A

It is a BiTE (Bispecific T cell engager) it directs CD8 T cells to destory the B cell. Wouldn’t work if the T cells were the problem

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10
Q

What are the two well known extramedullary presentations of AML?

A

Leukemia cutis and Myeloid Sarcoma (Chloroma)

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11
Q

ALL with ABL1, ABL2, CSF1R, PDGFRB fusions is a type of philadelphia-positive-like ALL sensitive to ______

A

Dasatinib

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12
Q

What is the dosing of HiDAC?

A

3g/m2 q12h as a bolus rather than infusional (i.e. infusional intermediate dose Ara-C is in 7+3)

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13
Q

What are some molecular mutations that guide therapy in AML with normal cytogenetics (5)?

A

NPM1, CEBPA, KIT, FLT3-ITD, FLT3-TKD

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14
Q

How should you manage a CR in Ph- ALL who achieve CR and have no MRD?

A

Can continue maintenance chemo; if MRD present or bad risk cytogenetics go with alloHSCT

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15
Q

How should all patients with FLT3-ITD be consolidated?

A

Consolidate with allo-HSCT; obviously if no donor can do HiDAC

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16
Q

What type of AML is associated with CD235a?

A

Erythroleukemia, M6

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17
Q

Who is Blinatumumab used in?

A

Blinatumumab is used in Philadelphia negative precursor B cell ALL who have refractory or relapsed disease

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18
Q

What type of ALL does NOT require maintenance?

A

Burkitt lymphoma does not require long maintenance period. But all other types require 2-3 year maintenance period.

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19
Q

Why would chronic GVHD lead to increased risk of infection with encapsulated organisms?

A

Can lead to hyposplenia and compromised splenic macrophage function; also often causes hypogammaglobulinemia

20
Q

ALL with ETV6-NTRK3 is a type of Philadelphia-positive-like ALL that is senstive to ______

A

Crizotinib (also used in ALK lung adeno)

21
Q

What is AML-M3v?

A

Hypogranular variant of APML (20% of APML)

22
Q

What do you do if you have a patient on Ara-C and they develop cerebellar toxicity which resolves?

A

Do NOT give another trial of cytarabine; consider another consolidative tx such as autoHSCT if good cytogenetics; allo if bad

23
Q

Which types of AML should have an LP performed during remission due to increased risk of CNS disease?

A

M4 (myelomonocytic) and M5 (monocytic) as well as Biphenotypic (myeloid + lymphoid features)

24
Q

What WBC count confers a higher risk of differentation syndrome in APML?

A

>10,000

25
Q

What type of AML causes gingival hyperplasia?

A

AML M5

26
Q

What are 3 favorable karyotypes in which HiDAC consolidation is preferred over allo-HSCT in AML?

A

t(8;21), inv(16) t(16;16)

27
Q

What are the two variants of APML?

A

M3 and M3v; Hypergranular and Hypgranular

28
Q

What CD marker is monocytic leukemia (M5) associated with?

A

CD11c, CD14 (Macrophage), and CD64; note that CD11c is also fairly specific for Hairy Cell Leukemia

29
Q

Why does the M5 subtype of AML often cause diffuse alveolar hemorrhage during induction phase of treatment?

A

M5 = acute monocytic leukemia so they have monocytic differentiation, they want to go to tissues to become MO so often cause gum and lung infiltration; when chemo started causes DAH

30
Q

Which purine analog showed a potential benefit in AML in one study?

A

Cladribine; fludarabine did not show benefit

31
Q

CD11c, CD14, and CD64 are associated with what type of AML? What other leukemia is assoc with CD11c?

A

M5 (Monocytic); Hairy cell leukemia

32
Q

How long is the maintenance tx of APML?

A

1-2 years often with ATRA, 6-MP, and MTX

33
Q

Which type of AML requires a long maintenance phase?

A

APML, there is induction, consolidation, and then a 1-2 year maintenance phase

34
Q

What is the general schematic for consolidation regimens of APML?

A

>2 cycles of anthracycline based therapy + 1-2 weeks ATRA +/- cytarabine

35
Q

Which type of AML is most likely to cause diffuse alveolar hemorrhage during induction chemo?

A

AML M5 because it is acute monocytic leukemia and goes to the lungs

36
Q

What is the general schematic for induction regimens in APML?

A

ATRA + Anthracycline +/- cytarabine

37
Q

What is AML M4?

A

Myelomonocytic Leukemia

38
Q

What type of leukemia is associated with CD41 + CD61?

A

M7- Megakaryoblastic leukemia

39
Q

What CD marker is associated with erythroleukemia (M6)?

A

CD235a

40
Q

This is the definition of complex cytogenetics in AML

A

More than 3 abnormalities

41
Q

The RATIFY study evaluated what drug in treatment of pts with newly diagnosed AML with FLT3 positivity?

A

Midostaurin

42
Q

What are the side effects of arsenic trioxide?

A

Can cause QTc prolongation due to blockage of potassium channels

43
Q

What is the general schematic for maintenance chemo in APML?

A

ATRA + 6-MP + MTX for 1-2 YEARS

44
Q

How does Blinatumumab work?

A

BiTE (Bispecific T cell engager) which directs CD8 T cells to destroy B cells. Does so by acting as a connector between CD3 on T cells and CD19 on B lymphoblasts; only used in philadelphia negative

45
Q

What is the major treatment difference between B cell and T cell ALL?

A

In T cell ALL, mediastinal irradiation may be beneficial but otherwise the Tx is the same, both require intrathecal ppx

46
Q

What is a long term side effect of topoisomerase II inhibitors?

A

Bone marrow damage leading to MDS 1-3 years after exposure because of rearrangements of the MLL gene (mixed lineage leukemia) @ 11q23 locus

47
Q

Intermediate risk cytogenetics for AML are what?

A

Normal cytogenetics, i.e. normal male or female karyotype

MALIGNANT HEME (12 decks)

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